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Biomedical subjects

C Giannini

Publications and source records attributed to C Giannini.

90 records · Page 5Linked to original sources
PubMed1992

Inherited neuroaxonal dystrophy in C6 deficient rabbits.

We report the occurrence of a progressive neurological syndrome clinically characterized by subacute motor neuropathy in offspring of C6 deficient rabbits. On the basis of the pedigree analysis, the disease appears to be genetically transmitted, most probably with an autosomal recessive mode of inheritance. Pathological studies of affected animals revealed: transmitted, most probably with an autosomal recessive mode of inheritance. Pathological studies of affected animals revealed: 1) severe axonal degeneration in the sciatic nerve system involving mainly motor fibers; 2) occasional peripheral axonal enlargement closely associated with axonal degeneration; 3) presence of structured abnormal material in normal-size myelinated fibers of central nervous system (CNS) and peripheral nervous system (PNS); and 4) widespread occurrence of dystrophic axons and axonal spheroids in the gray matter of CNS. By ultrastructural examination, dystrophic axons are filled with tubulovesicular material, stalks of parallel membranes and dense bodies similar to what is described in human neuroaxonal dystrophies (NAD). The disease manifested by C6 deficient rabbits may represent an animal model of primary human NAD.

Animals↗
PubMed1990

Polyglucosan body axonal enlargement increases myelin spiral length but not lamellar number.

The area of the unrolled myelin sheet of internodes of myelinated fibers (MF) of peripheral nerve is thought to be determined by axonal caliber and internodal length. We studied the effect of a focal increase of axonal caliber due to the deposition of polyglucosan bodies (PGB), amylopectin-like glucose polymers, on number of myelin lamellae (NL), interlamellar distance (periodicity), and myelin spiral length (MSL) from a sural nerve biopsy specimen of a patient with chronic inflammatory demyelinating polyneuropathy. Axonal area, NL, periodicity, and MSL were estimated within internodes of MF above, at, and below PGB. The axon caliber at the level of the PGB was significantly (P less than 0.002) increased when the PGB was included. At the PGB, NL and their periodicity were not significantly different from those above or below the PGB. The MSL was significantly longer overlying the PGB than it was in the same internode above or below the PGB. Because slippage or stretching of the myelin sheath as well as movement of molecular constituents of myelin is not likely over large distances, localized biosynthesis and assembly of new myelin may explain this increase of MSL.

Axons↗
PubMed1990

Myokymic syndrome with impaired muscular relaxation: further evidence of a possible paraneoplastic genesis.

A case of concomitant myokymia with impaired muscular relaxation and hypertrophic osteoarthropathy associated with the presence of two separate lung malignancies is described. Both the neurological syndrome and osteoarticular disorder significantly improved after surgical removal of the lung cancers. The possibility that common mechanisms may underlie these two tumour-related disorders is also discussed.

Adenocarcinoma↗
PubMed1990

Structural alterations of nerve during cuff compression.

Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure- and time-related structural changes observed in the present study under the cuff were (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (ii) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement of layers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.

Animals↗
PubMed1990

The fate of Schwann cell basement membranes in permanently transected nerves.

After peripheral nerve fiber degeneration, Schwann cell basement membranes (SCBM) persist, maintain the columnar orientation of multiplying Schwann cells, and provide pathways for regenerating axons to original target tissue. Despite the putative importance of these functions, there is little quantitative information on SCBM in chronic denervation. The number, integrity, shape, and size of SCBM were evaluated in transverse electron micrographs of peroneal nerves of groups of mice at various times after permanent sciatic nerve transection. With increasing time after transection, the SCBM fragment, the fragments become shorter, dispersed throughout the endoneurium and partially disappear. The discontinuity, dispersion, and partial disappearance of SCBM, which worsens with time after nerve transection, alters the scaffold by which neurites grow back to formerly innervated or appropriate target tissue. Without reaching appropriate target tissue, regenerating fibers may fail to develop or undergo retrograde atrophy and degeneration. The progressive changes of the SCBM may contribute to the demonstrated poor regeneration when nerve reconnection is delayed, or when proximal nerves are reconnected, so that much time may elapse before neurites grow back to distal nerve.

Animals↗
PubMed1989

Number, size, and class of peripheral nerve fibers regenerating after crush, multiple crush, and graft.

Morphometric characterization of fiber regeneration in a distal nerve after focal proximal nerve injury may provide useful clinical information and insights about underlying neurobiologic mechanisms. The myelinated (MF) and unmyelinated (UF) fibers of peroneal nerve of groups of mice were assessed 9 months after crush, graft, and multiple crush injury of the proximal sciatic nerve: number and size distribution of axon areas, myelin areas, and fiber diameters. After crush, number of regenerated MF and UF was almost identical to that of controls. Their size distribution had almost returned to normal. After graft and multiple crush, fiber number had returned to normal or was significantly increased beyond normal but there were only a few large fibers present. This may be explained by: (a) disproportionate regeneration of small-diameter compared to large-diameter classes of fibers; (b) misdirected regrowth of fibers, so that functional reinnervation was not established, resulting in failure of development or retrograde atrophy and degeneration; or (c) cellular alterations at the site of injury or in the distal nerve which inhibited neural outgrowth or elongation or did not inhibit outgrowth but retarded or prevented maturation. We conclude that explanation (b) is involved, and that there is some evidence favoring the roles of (a) and (c).

Animals↗
PubMed1989

Resistance to axonal degeneration after nerve compression in experimental diabetes.

To determine the effect of diabetes on the development of axonal degeneration after acute nerve compression, the mobilized peroneal nerves of rats with streptozotocin-induced diabetes and of control rats were compressed at 150 mmHg (1 mmHg = 133 Pa) for 30 min by using specially devised cuffs. At three intervals after compression--3 days, rats diabetic for 31 wk; 14 days, diabetic for 6 wk; and 24 days, diabetic for 31 wk--groups of nerves were studied to assess numbers and sizes of fibers above, at, and below the cuff and to assess frequency of fiber degeneration in teased fibers from nerve distal to the cuff. Teased fibers with pathologic abnormalities were more frequent in nerves from controls than in nerves from diabetic rats in all three groups but the difference was statistically significant only at 3 and 14 days after compression. The lack of significant difference at 24 days may be explained by higher rates of disappearance of degenerating products and of fiber regeneration at 24 than at 3 and 14 days. This study provides evidence that in addition to delaying the reported functional deficit of vibratory detection threshold and conduction block during nerve compression, diabetes also may partially prevent axonal injury. Low nerve myo-inositol concentration did not predispose diabetic nerve to acute compression injury. If these results also apply to human diabetes and if repeated acute compression is involved in the genesis of fiber degeneration in entrapment, then a higher frequency of entrapment neuropathy among diabetics might be due to mechanisms other than increased susceptibility of fibers to acute compression--e.g., possibly to greater constriction of nerve due to pathologic alterations of the carpal ligament.

Animals↗
PubMed1988

Polyneuropathy in hypereosinophilic syndrome.

We investigated two patients with the idiopathic hypereosinophilic syndrome and peripheral neuropathy. Clinical, EMG, and pathological findings were consistent with axonal polyneuropathy. Morphologic changes of the nerve biopsies suggested axonal damage secondary to increased endoneurial pressure from leakage of capillaries. We postulate that endothelial cell damage, followed by nerve edema, is the first step in the pathogenesis of peripheral neuropathy in these patients.

Biopsy↗
PubMed1985

The role of the tactile-pressure afferents in the habituation phenomenon of trigemino-facial reflex.

In ten healthy subjects the trigemino-facial reflex was elicited by double shock (delta t = 0.5-1 s). The first stimulus was subliminal for pain and the second supramaximal for it. The percentage integral values, with respect to single shock, of the direct and consensual conditioned responses obtained in all subjects were averaged and compared with those conditioned by supramaximal stimuli for pain fibres. Significant differences between subliminal and supramaximal conditioning stimuli for pain fibres is revealed for only consensual R3 with delta t = 1 s: greater inhibition with painful stimuli. There were no significant differences in any of the other values. Our results show that a subliminal conditioning stimulus for pain threshold can inhibit the late responses to the test stimulus, both for R2 and especially for R3, suggesting that this mechanism can contribute to the trigemino-facial reflex habituation phenomenon.

Electrophysiology↗
PubMed1983

Prenatal education for the Spanish speaking: an evaluation.

A Spanish-language prenatal health-education program of classes in four topic areas was conducted for randomly selected pregnant women. The topics included newborn care, labor and delivery, family planning, and dental health care. A questionnaire was administered to the participants after they had attended all four sessions and at the end of their 36th week of gestation. A matched group of control women received the same questions soon after entering the program and before attending any classes. Women attending the health-education classes demonstrated significantly greater knowledge of the subjects covered than did those not taking the classes. Insights gained from the study suggest potential approaches for working with such a population with respect to cultural considerations, evaluation question construction, and question selection.

California↗
PubMedDate not supplied

Ultrastructural features of pleomorphic xanthoastrocytoma: a comparative study with glioblastoma multiforme.

Eighteen tumors (15 cases) were ultrastructurally examined and compared to 11 examples of glioblastoma multiforme (GBM) [to determine the cellular nature of pleomorphic xanthoastrocytoma (PXA).] PXA, as well as GBM, were principally composed of pleomorphic astrocytes containing numerous intermediate filaments. Lipid droplets, lysosomes, and basal laminas were more numerous and fully developed in PXA, but were not specific to the tumor. Aggregates of secondary lysosomes, light microscopically evident as eosinophilic granular bodies, and ribosome-lamella complexes were exclusively seen in PXA. Also noted in PXA were centrioles, occasional Rosenthal fibers, hemidesmosomes in small number, rudimentary cell junctions, and interstitial calcifications. In addition to astrocytic constituents, 20% of PXA contained cells with neuronal features, as evidenced by the presence of dense-core granules, microtubules, and clear vesicles. In contrast, GBMs consisted solely of astrocytic cells. In the present study, the salient ultrastructural findings of PXA were largely degenerative in nature, including numerous lipid droplets and secondary lysosomes, as well as basal laminas, ribosome-lamella complexes, and occasional neuronal differentiation. The presence of basal lamina does not necessarily imply a histogenetic derivation from subpial astrocytes, in that it is also a common feature of GBM. Given the occurrence of biphenotypic, glioneuronal differentiation in some cases, PXA may be derived from a neuroepithelial stem cell. The authors conclude that PXA is fundamentally an astrocytic tumor, albeit one with a significant tendency to undergo neuronal differentiation.

Astrocytes↗
PubMedDate not supplied

Evidence of neuromuscular hyperexcitability features in patients with primary fibromyalgia.

The presence of clinical and electromyographic (EMG) features of neuromuscular hyperexcitability (NMHE) and of the commonly associated neurovegetative disturbances (NVD) were investigated in 49 patients with primary fibromyalgia (PF) and in a control group of 33 patients with rheumatoid arthritis (RA). At least two clinical features of NMHE were present in 39%, and at least three NVD in 63% of PF patients. In contrast, only 1 RA control had two NMHE features (p greater than 0.005) and three NVD (p less than 0.001). Moreover, a significant post-ischemic spontaneous EMG hyperactivity was observed in 11 PF patients, and in only 1 control with RA (p less than 0.05). Finally, in patients with PF the number of tender points were correlated with psychological tests for depression (p less than 0.02), and the number of NVD. The present study shows that in patients with PF there is a large prevalence of NMHE complaints and NVD. The potential underlying pathogenetic mechanisms are also discussed.

Adolescent↗
PubMedDate not supplied

Neuroelectric procedure does not discriminate between painful and paresthetic diabetic neuropathy.

To investigate whether pain and paresthesias could identify two different subclasses of small-fibre diabetic neuropathy, and to evaluate their relation to the metabolic control, we tested nerve conduction velocity (NCV) of median nerve (sensitive-SM, and motor-MM) and deep peroneal nerve (DP) in 48 diabetics (24 IDDM, 24 NIDDM) reporting pain (group A) or paresthesias (group B) that might be due to diabetic polyneuropathy. Glycated haemoglobin (HbA1c) was also assessed. No difference between group A and group B was found either in NCV, in all nerves tested, or in HbA1c. No relation was observed between NCV of nerves tested and HbA1c, duration of diabetes, age and type of diabetes in both groups.

Adult↗
PubMedDate not supplied

Hepatitis C virus as a lymphotropic agent: evidence and pathogenetic implications.

Hepatitis C virus has been proven to be the major cause of NANB hepatitis, cirrhosis and hepatocellular carcinoma worldwide. Based on the genome similarities between HCV and flavivirus or pestivirus, this agent has been included within the family Flaviviridae as a separate genus. Among the analogies between HCV and the other members of the same family there is the possibility of infecting blood cells. In particular, significant evidence obtained through studies performed in vivo and in vitro support the concept that HCV is not only a hepatotropic but also a lymphotropic virus. This suggests that, in addition to playing a role in inducing hepatic diseases (both of a non-tumoral and a neoplastic nature), HCV infection may also play a role in extrahepatic pathologies. The striking association observed between HCV infection and some autoimmune-lymphoproliferative disorders of either benign or neoplastic nature is consistent with this hypothesis. However, in analogy with what has been observed in the case of liver disease, the mechanisms involved in the pathogenesis of HCV-related extra-hepatic manifestations have to be more deeply analysed and clarified.

B-Lymphocytes↗